414 CHAPTER 9 Upper tract obstruction
Pathophysiology of urinary tract obstruction
Effects of obstruction on renal blood flow and ureteric pressure
Acute unilateral obstruction of a ureter (UUO)
This leads to a triphasic relationship between renal blood flow (RBF) and ureteric pressure.
•Phase 1 (up to 1.5 hours post-obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation)
•Phase 2 (1.5–5 hours post obstruction): ureteric pressure continues to rise, RBF falls (efferent arteriole vasoconstriction)
•Phase 3 (beyond 5 hours): ureteric pressure falls, RBF continues to fall (afferent arteriole vasoconstriction)
Acute bilateral obstruction of a ureter (BUO) or obstruction of a solitary kidney
•Phase 1 (up to 1.5 hours post-obstruction): ureteric pressure rises, RBF rises (afferent arteriole dilatation)
•Phase 2 (1.5–5 hours post-obstruction): ureteric pressure continues to rise, RBF is significantly lower than that during unilateral ureteric obstruction
•Phase 3 (beyond 5 hours): ureteric pressure remains elevated (in contrast to UUO). By 24 hours, RBF has declined to the same level as or both unilateral and bilateral ureteric obstruction.
In UUO, the decrease in urine flow through the nephron results in a greater degree of Na absorption, so Na excretion falls. Water loss from the obstructed kidney increases.
Release of BUO is followed by a marked natriuresis, increased K excretion, and a diuresis (a solute diuresis). This is due to the following:
•An appropriate (physiological) natriuresis, to excrete excessive Na that is a consequence of BUO
•A solute diuresis from the accumulation of urea in extracellular fluid
•A diminution of the corticomedullary concentration gradient, which is normally established by the countercurrent mechanism of the loop of Henle, and is dependent on maintenance of flow through the nephron. Reduction of flow, as occurs in BUO, reduces the efficiency of the countercurrent mechanism (effectively, the corticomedullary concentration gradient is washed out).
There may also be accumulation of natriuretic peptides (e.g., ANP) during BUO, which contributes to the natriuresis following release of the obstruction.
PATHOPHYSIOLOGY OF URINARY TRACT OBSTRUCTION 415
Likelihood of recovery of renal function after release of obstruction
In dogs with completely obstructed kidneys, full recovery of renal function after 7 days of UUO occurred within 2 weeks of relief of obstruction. After 14 days of obstruction there was a permanent reduction in renal function to 70% of control levels (recovery to this level taking 3–6 months after reversal of obstruction).
There is some recovery of function after 4 weeks of obstruction, but after 6 weeks of complete obstruction there is no recovery. In humans, there is no clear relationship between the duration of BUO and the degree of recovery of renal function after relief of obstruction.
416 CHAPTER 9 Upper tract obstruction
Physiology of urine flow from kidneys to bladder
Urine production by the kidneys is a continuous process. Its transport from the kidneys, down the ureter, and into the bladder occurs intermittently, by waves of peristaltic contraction of the renal pelvis and ureter (peristalsis = wavelike contractions and relaxations). The renal pelvis delivers urine to the proximal ureter. As the proximal ureter receives a bolus of urine it is stretched, and this stimulates it to contract, while the segment of ureter just distal to the bolus of urine relaxes. Thus the bolus of urine is projected distally.
The origin of the peristaltic wave is from collections of pacemaker cells in the proximal-most regions of the renal calyces. In species with multiple calyces, such as humans, there are multiple pacemaker sites in the proximal calyces.
The frequency of contraction of the calyces is independent of urine flow rate (it is the same at high and low flow rates) and it occurs at a higher rate than that of the renal pelvis. Precisely how frequency of contraction of each calyx is integrated into a single contraction of the renal pelvis is not known.
All areas of the ureter are capable of acting as a pacemaker. Stimulation of the ureter at any site produces a contraction wave that propagates proximally and distally from the site of stimulation, but under normal conditions, electrical activity arises proximally and is conducted distally from one muscle cell to another (the proximal most pacemakers are dominant over these latent pacemakers).
Peristalsis persists after renal transplantation and denervation and does not therefore appear to require innervation. The ureter does, however, receive both parasympathetic and sympathetic innervation, and stimulation of these systems can influence the frequency of peristalsis and the volume of urine bolus transmitted.
At normal urine flow, the frequency of calyceal and renal pelvic contractions is greater than that in the upper ureter, and there is a relative block of electrical activity at the UPJ. The renal pelvis fills; the ureter below it is collapsed and empty. As renal pelvic pressure rises, urine is extruded into the upper ureter. The ureteric contractile pressures that move the bolus of urine are higher than renal pelvic pressures.
A closed UPJ may prevent back-pressure on the kidney. At higher urine flow rates, every pacemaker-induced renal pelvic contraction is transmitted to the ureter.
To propel a bolus of urine, the walls of the ureter must coapt (touch). Resting ureteric pressure is ~0–5 cmH2O and ureteric contraction pressures range from 20 to 80 cmH2O.
Ureteric peristaltic waves occur 2–6 times per minute. The VUJ acts as a one-way valve under normal conditions, allowing urine transport into the bladder and preventing reflux back into the ureter.
URETER INNERVATION 417
Ureter innervation
Autonomic
The ureter has a rich autonomic innervation.
•Sympathetic—preganglionic fibers from spinal segments T10 to L2; postganglionic fibers arise from the celiac, aorticorenal, mesenteric, superior and inferior hypogastric (pelvic) autonomic plexuses
•Parasympathetic—vagal fibers via celiac to upper ureter; fibers from S2–4 to lower ureter
The role of ureteric autonomic innervation is unclear. It is not required for ureteric peristalsis (though it may modulate this). Peristaltic waves originate from intrinsic smooth muscle pacemakers located in minor calyces of renal collecting system.
Afferent
•Upper ureter—afferents pass (alongside sympathetic nerves) to T10–L2
•Lower ureter—afferents pass (alongside sympathetic nerves and by way of pelvic plexus) to S2–4.
Afferents subserve stretch sensation from the renal capsule, collecting system of kidney (renal pelvis and calyces), and ureter. Stimulation of the mucosa of the renal pelvis, calyces, and ureter also stimulates nociceptors, the pain felt being referred in a somatic distribution to T8–L2 (kidney T8–L1, ureter T10–L2), in the distribution of the subcostal, iliohypogastric, ileoinguinal, or genitofemoral nerves.
Thus, ureteric pain can be felt in the flank, groin, scrotum or labia, and upper thigh, depending on the precise site in the ureter from which the pain arises.
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